Changes in albumin, α-fetoprotein and collagen gene transcription in ccl4-induced hepatic fibrosis
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In efforts to understand mechanisms of liver dysfunction in cirrhosis, transcription of specific genes important to liver function has been measured in the rat model of CCl 4 -induced hepatic fibrosis. The relative transcription rates of albumin, α-fetoprotein and pro-α 1 -collagen genes were studied during development of fibrosis and after fibrosis was established. During the initial phase of CCl 4 administration, there was a decrease in albumin transcription associated with increased α-fetoprotein transcription, indicative of active liver regeneration. However, later during development of fibrosis, the response pattern of these genes was different, as albumin gene transcription was normal or increased and α-fetoprotein gene transcription was no longer increased. Three weeks after completion of CCl 4 treatment (fully established cirrhosis), albumin genes responded normally or hypernormally to an acute regenerative stimulus, but the α-fetoprotein gene was again not measurably responsive. Pro-α 1 -collagen gene transcription increased during the entire fibrogenic process and remained elevated after cirrhosis was established. These studies suggest that a switch from albumin to α-fetoprotein gene transcription can serve as a marker of liver regenerative capacity, and that this process is altered during and after development of hepatic fibrosis. The fibrogenic process is also associated with elevated transcription of collagen genes.Keywords:
Transcription
Hepatic fibrosis
CCL4
Liver Regeneration
CCL4
Hepatic fibrosis
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The connective tissue growth factor(CTGF) can enhance the proliferation of fibroblasts and promote the extra cellular matrix synthesis.It is an important cytokine that can promote organ fibrosis.There is a strong correlation between the CTGF and hepatic fibrosis.The CTGF expression of human hepatic fibrosis,cirrhosis and experimental hepatic fibrosis model is significantly rising.The inhibition of CTGF expression can reduce the extra cellular matrix synthesis,resulting in the inhibition of hepatic fibrosis.The further study of CTGF is important for the pathogenesis,therapeutic mechanism and the clinical treatment of hepatic fibrosis and cirrhosis.In the review,the function of CTGF and its state on the pathogenic process,diagnosis and treatment of hepatic fibrosis were summarized and discussed.
Hepatic fibrosis
Hepatic stellate cell
Pathogenesis
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Objective To observe the antifibrotic effects of chelerythine in rats with CCl4-induced hepatic fibrosis.Methods Hepatic fibrosis models in rats were established by injection of tetrachloride,in combination with the control of nutrition and the drinking 10% of alcohol.Four weeks later,chelerythine and γ-interferon were used in two groups respectively,for comparison to control and fibrotic model group.At the end of eight weeks,the histological changes and hydroxyproline content were detected.Result The pathological fibrosis scores and liver hydroxyproline content in rats with chelerythine or γ-interferon intervention decreased significantly as compared with fibrotic model group(P0.01),and the effect of chelerythine was found to be in a dose-dependent manner.Conclusions Chelerythine can improve the hepatic injuries in rats with tetrachloride-induced hepatic fibrosis.
Hydroxyproline
CCL4
Hepatic fibrosis
Rat model
Tetrachloride
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Objective To find the best model of hepatic fibrosis.Methods Wistar rats were randomly allocated into three groups:pig serum group (n=30),subcutaneous injection carbon tetrachloride (CCl4) group (n=30) and intraperitoneal injection CCl4 group (n=30).Hepatic fibrosis was induced by subcutaneous,intraperitoneal injection of 40% CCl4 or pig serum (two times per a week) for 4 weeks and 6 weeks respectively in rats.Rat mortality,change of liver tissue and degree of hepatic fibrosis in all groups were examined.Results Hepatic fibrosis models were induced successfully by the three different methods,but rat mortalities in the pig serum group and 40% CCl4 subcutaneous injection group were significantly lower than in 40% CCl4 intraperitoneal injection group,and the time of hepatic fibrosis model formation in the 40% CCl4 group was shorter obviously than that in the other two groups.Conclusion Hepatic fibrosis induced by subcutaneous injection CCl4 is the best model of hepatic fibrosis.
CCL4
Subcutaneous injection
Intraperitoneal injection
Hepatic fibrosis
Animal model
Rat model
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Astragaloside (AGS) extracted from radix astragalin (Huangqi) has been considered to be beneficial to liver diseases. In this study, we examined the role played by AGS in alleviating hepatic fibrosis function via protease-activated receptor-2 (PAR2) mechanisms. We hypothesized that AGS affects PAR2 signaling pathway thereby improving hepatic function in rats with hepatic fibrosis induced by carbon tetrachloride (CCl4). We further hypothesized that AGS attenuates impaired hepatic function evoked by CCl4 to a greater degree in diabetic animals.ELISA and Western Blot analysis were used to examine PAR2 signaling pathway in diabetic CCl4-rats and non-diabetic CCl4-rats.AGS inhibited the protein expression of PAR2 and its downstream pathway PKA and PKCɛ in CCl4-rats. Notably, the effects of AGS were greater in CCl4-rats with diabetes. AGS also significantly attenuated the CCl4-induced upregulations of pro-inflammatory cytokines, namely interleukin-1β, interleukin-6 and tumor necrosis factor-α accompanied with decreases of collagenic parameters such as hexadecenoic acid, laminin and hydroxyproline. Additionally, AGS improved the CCl4-induced exaggerations of liver index and functions including alanine aminotransferase, aspartate aminotransferase. Moreover, TGF-β1, a marker of hepatic fibrosis, was increased in CCl4-rats and AGS inhibited increases in TGF-β1 induced by CCl4.AGS alleviates hepatic fibrosis by inhibiting PAR2 signaling expression and its effects are largely enhanced in diabetic animals. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of hepatic fibrosis; and results of our study are likely to shed light on strategies for application of AGS because it has potentially greater therapeutic effectiveness for hepatic fibrosis in diabetes.
Hepatic fibrosis
CCL4
Hepatic stellate cell
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CCL4
Hepatic fibrosis
Hepatic stellate cell
Procollagen peptidase
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CCL4
Hepatic fibrosis
Hepatotoxin
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This work was undertaken to establish a new experimental model of hepatic fibrosis by gamma irradiation and CCl4 and to study the hepatoprotective effect of Reishi Mushroom (RM) against hepatic fibrosis induced in that model. Our results revealed that oral co-administration of 110 mg/kg RM by gavage to fibrotic rats offered an obvious hepatic protection as assured by the significant decrement in ALT and AST, HP content, MDA and NO levels with elevation of the antioxidant enzymes activities. The levels of TGF-β, TNF-α, HO-1 and type-1 collagen and their m-RNA expression were markedly declined as compared with those of fibrotic rats. Microscopical examination revealed that the exposure of rats to radiation aggravated the effect of CCl4 causing extensive collagen deposition and marked pseudolobulation of the hepatic parenchyma indicative of bridging fibrosis. While, oral co-administration of RM obviously improved the state of steatosis and apparently suppressed hepatic fibrogenesis.
CCL4
Hepatic fibrosis
Steatosis
Hepatic stellate cell
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ObjectiveTo study the approaches for making acute hepatic failure model on chronic hepatic damage in rat.MethodsSD rats were intraperitoneally injected with 50% CCl4(Carbon tetrachloride) olive solution every three days for three months.And SD rats had been injected with a dose of 1.5 mL/kg BW(body weight) for one month while 2.0 mL/kg BW for next two months.Then they were divided into three groups randomly and injected with D-galactosamine at a dose of 2 g/kg BW,lipopolysaccharide at a dose of 100 μg/kg BW and D-galactosamine at a dose of 0.5 g/kg BW,50% CCl4 olive solution at a dose of 5 mL/kg BW respectively.The levels of serum ALT,AST and TBil were detected by observing SD rats' diet and BW.And histopathological changes were observed to evaluate these three models.ResultsAfter injection of 50% CCl4 olive solution intraperitoneally for 3 months,hepatic damage happened in SD rats,including liver fibrosis,cirrhosis,ascites and jaundice.Acute hepatic failure was quickly induced administration of three reagents mentioned above.ConclusionBy injecting of 50% CCl4 olive solution intraperitoneally,acute hepatic failure model on chronic hepatic damage model could be induced by D-galactosamine,lipopolysaccharide or D-galactosamine and CCl4 in rats.
CCL4
Hepatic fibrosis
Galactosamine
Hepatic dysfunction
Chronic hepatic
Acute hepatic failure
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OBJECTIVE To investigate the protective effect of baicalin against carbon tetrachloride( CCl4)-induced hepatic fibrosis in mice.METHODS The experimental model mice of hepatic fibrosis was induced by CCl4.The serum ALT/GPT,AST/GOT,AKP, hepatic hydroxyproline ( HYP) and liver,spleen and thymus index were determined.RESULTS Baicalin significantly reduced serum ALT/GPT,AST/GOT,AKP,HYP and liver index.CONCLUSION Baicalin has a protective effect on hepatic fibrosis induced by CCl4 in mice.
Baicalin
Hydroxyproline
CCL4
Hepatic fibrosis
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